Managing insomnia in the primary care setting

This is a common condition.

T Henderson, MB ChB, FCPsych (SA)

Senior Registrar, Department of Psychiatry, University of Cape Town

Terri
Henderson worked as a senior specialist psychiatrist in general adult
and adolescent psychiatry at Lentegeur Hospital, Mitchell’s Plain, Cape
Town, before joining the Division of Child and Adolescent Psychiatry at
Red Cross Hospital as a senior registrar in August 2011.

Correspondence to: T Henderson (thenders@pgwc.gov.za)

Primary insomnia is a common condition, occurring at a rate of approximately 10% in its chronic form in the general population.1
It often starts with a specific problem, such as loss of a job, or a
change in sleep patterns, e.g. with childbirth. It is often co-morbid
with other psychiatric disturbances where the insomnia predates the
other psychiatric symptoms.2
Advancing age is associated with reduced amount of sleep, reduced sleep
efficiency and more awakenings. Women are twice as likely to develop
insomnia as men. The condition becomes chronic when perpetuated by the
following factors: anxiety about sleep, maladaptive sleep habits,
underlying vulnerability in sleep-regulating mechanisms and persistence
of the precipitant stressor.2

Diagnosing insomnia

Primary insomnia refers to a sleep disturbance that is not
associated with a causative underlying condition. The ICD-10 diagnostic
criteria for insomnia are listed in Table 1. Diagnosing insomnia
requires a thorough sleep, medical, drug, alcohol, substance and
psychiatric history.1,3
The sleep history has to identify factors that precipitated the
insomnia, current life stressors, a description of a typical 24-hour
period of sleep behaviour, which strategies have been tried to correct
the sleep disturbance and to what extent such strategies were
successful.1
Most clinicians consider >30 minutes to fall asleep and/or ≥30
minutes of wakefulness after sleep onset and total sleep time of
<6.5 hours per night to represent the threshold between normal and
abnormal sleep.1
The detrimental effects of insomnia include: reduced quality of life,
subjectively impaired cognitive performance, decreased ability to
handle minor irritations and to enjoy family and social life, an
increase in risk for a first episode of or relapse in depression,
increased risk for substance abuse, hypertension, absenteeism, chronic
feelings of over-arousal, road traffic accidents and activation of the
hypothalamic-pituitary axis.1,2 Commonly prescribed drugs that cause insomnia are listed in Table 2.

Differential diagnoses

Secondary insomnia differs from primary insomnia in that a
specific condition can be identified as the cause of the sleep problem.
Diagnostic tests for sleep disorders include oximetry and
polysomnography. They are useful in detecting causes of secondary
insomnia. Circadian rhythm disorder is a common condition manifested as
misalignment between the sleep period and the physical/social 24-hour
environmental cycle.4
Delayed sleep phase (typical in adolescents) and advanced sleep phase
(frequent in the elderly) are the two most prevalent circadian rhythm
sleep disorders.4
Others include jet lag and shift work disorder. Parasomnias are unusual
episodes or behaviours that occur during sleep and disturb the patient
or others. They include non-REM and REM disorders. Non-REM disorders
include night terrors and sleepwalking. Night terrors are the abrupt
awakening from deep non-REM sleep, usually during the first third of
the night, often with a scream or signs of intense fear. Patients are
unresponsive to comforting, difficult to wake, appear confused and have
no recall of the experience. It is common in children but also occurs
in adults and has a strong genetic component.2
Sleepwalking often occurs in addition to night terrors where patients
perform highly familiar behaviours such as walking or dressing and are
difficult to wake. REM disorders include nightmares and REM sleep
behaviour disorder (RBD). Unlike non-REM disorders, patients with
nightmares can be woken and can recall the experience. They are common
in children and reassurance about safety is paramount. RBD presents as
a lack of atonia during REM sleep and an increased vividness of dreams.2
Narcolepsy is characterised by excessive daytime sleepiness, an
irresistible desire to fall asleep and the feeling of being refreshed
after daytime sleep.3
Symptoms occurring in the early evening when the patient is lying in
bed or at sleep onset may suggest a diagnosis of restless leg syndrome
(RLS).3
Repeated awakenings throughout the night, snoring and cessation of
breathing during sleep may suggest a diagnosis of obstructive sleep
apnoea syndrome (OSAS).3

Sleep-wake function

Two separate systems maintain sleep and wakefulness respectively.
Projections from the brainstem to the thalamus and forebrain using
noradrenalin, serotonin, acetylcholine, dopamine and the histamines
maintain arousal.2
The promotion of sleep is initiated by GABA, adenosine, melatonin and
the circadian pacemaker. Benzodiazepines target the GABA A receptor.
Adenosine acts at the adenosine A2
receptor. Adenosine levels rise during the day and peak levels are
associated with sleepiness. Caffeine causes insomnia by blocking this
mechanism.2
Melatonin is a hormone secreted from the pineal gland and regulates
circadian rhythm. The circadian pacemaker is located in the
suprachiasmatic nucleus of the hypothalamus and drives melatonin
synthesis.2

Treatment for insomnia

Insomnia that creates significant distress, with daytime symptoms,
warrants intervention. Before initiating treatment, ensure good sleep
hygiene practices (Table 3). Ensure that other psychiatric disorders
are adequately treated and medications causing insomnia have been
excluded. Typical exclusions for initiating insomnia treatment include
untreated or unstable medical, psychiatric or substance abuse
conditions.1
For the majority of patients with acute insomnia spontaneous recovery
does indeed occur. However, acute episodes that last 2 - 4 weeks may
develop into chronic insomnia. Therefore, early intervention is
warranted.1 Referral to a sleep specialist with failure of two treatment trials and/or diagnostic tests are required.

Medication

The selective benzodiazepine receptor agonists (BZRAs), zopiclone
and zolpidem, are chemically similar to the benzodiazepines and were
developed as hypnotic agents with a shorter half-life to avoid a
hangover effect. Zopiclone, prescribed at a dose of 7.5 mg, has a
longer half-life of approximately 6 hours and is useful for patients
who wake throughout the night. Zolpidem, prescribed at a dose of
10 mg, is useful for sleep-onset difficulties. Initiation of a
hypnotic effect is approximately 20 minutes; therefore BZRAs must be
taken when already in bed to avoid amnesia and motor effects. There are
many benzodiazepines available; lorazepam 1 - 2 mg (half-life 10 -
20 hours) and oxazepam

10 -15 mg (half-life 6 hours) are potential options. Tolerance
and dependence with long-term benzodiazepine use is well established
but is more controversial with the BZRAs. The original consensus was
that they should be used for a limited period of 2 - 3 weeks based on
the original trials conducted over this limited time period.2
In reality, many patients are on chronic treatment. Tolerance does not
seem to be a significant problem and many patients use the same dose
for months and still report these medications to be effective.2
However, chronic use may be associated with adaptive changes in
receptors and a withdrawal syndrome occurs that includes the following
symptoms: agitation, prolonged sleep-onset latency, headache,
irritability, hypersensitivity to stimuli, nausea, vomiting and
depersonalisation.2
Many patients develop a psychological dependence and are unwilling to
stop treatment. To avoid the development of dependence, strategies
include not administering the drug every night from the beginning of
treatment or periodic attempts at tapering and discontinuing medication
and the co-administration of cognitive behavioural therapy techniques.2

Sedating antidepressants are a good option for the long-term
maintenance treatment of insomnia, even in the absence of a major
depressive disorder, and there are no restrictions on duration of use.
The selective serotonin re-uptake inhibitors (SSRIs) disrupt sleep,
except for paroxetine in those over the age of 55 years. Trazodone at a
minimum dose of 50 mg may be beneficial for insomnia; side-effects
include sedation and postural hypotension. Mirtazepine (15 - 45 mg) and
mianserin (30 - 90 mg) are also useful as sedating antidepressants.
Both are associated with weight gain and sedation. Mianserin carries a
risk of neutropenia and requires measurement of the white cell count
(WCC) before initiation. Low-dose amitriptyline (10 mg or 25 mg) has a
long record of successful use but is contraindicated in suicidal
patients or in those with cardiac risk factors. SSRIs and tricyclic
antidepressants should not be used simultaneously (unless initiated and
carefully monitored, preferably by a specialist) as SSRIs inhibit
tricyclic metabolism which can lead to toxic levels of the latter.
Antidepressants should be prescribed at therapeutic doses when insomnia
coexists with a mood disorder.

Other medications

Over-the-counter medications include antihistamine compounds such as
diphenhydramine and doxylamine. These are only suitable for short-term
use and are minimally effective. Melatonin is particularly beneficial
in patients over the age of 55 years and is available as 3 - 5 mg
tablets without prescription, although the actual amount required is
probably 0.5 mg. It should be taken one hour before bedtime or at
bedtime. It has the benefit of no memory or motor effects in addition
to improved daytime outcomes. However, research on its long-term
effects is not available. It increases the risk of blood clotting and
should not be used with warfarin. It reduces the effectiveness of
antihypertensives and should be avoided in depressed patients. The
antipsychotics olanzapine and quetiapine have beneficial sedating
qualities but their side-effect profile of weight gain, diabetes and
lipid abnormalities make them unsuitable for use in insomnia. The
antihistamines only block one of the arousal systems and are therefore
largely ineffectual.

Cognitive-behavioural therapy (CBT)

CBT has shown good efficacy, requires approximately six sessions and
focuses on sleep-interfering behaviour, sleep hygiene, reduction of
hyper-arousal features and improvement of circadian rhythm with sleep
scheduling and partial sleep deprivation. An assessment for CBT
includes a detailed history of sleep, a medical and mental health
history, and placing an emphasis on factors that contribute to the
initiation and maintenance of insomnia. The patient is requested to
keep a sleep diary to document time to bed, time out of bed, minutes to
fall asleep (latency) and minutes awake during time in bed. The order
of treatment interventions includes sleep education, stimulus control
therapy, sleep restriction and relaxation training.5

Patients often feel that staying in bed when awake is beneficial,
but it ultimately creates conditioned arousal. The belief that
extending sleep opportunity to improve insomnia often results in more
frequent and longer awakenings. Stimulus control therapy addresses
incorrect assumptions (Table 4).5

Sleep restriction therapy requires estimation of a sleep average
over a 2-week period by calculating the number of hours of sleep an
individual gets per night. A fixed wake time is established and a sleep
window is calculated to which 30 minutes is added. A sleep diary is
recorded and the sleep window is adjusted by 30 minutes as sleep
efficiency improves. For example, if a patient sleeps six hours per
night and sets a waking time of 06h00, they go to bed at 23h30. As
sleep efficiency improves, they add an additional 30 minutes to the
bedtime, which then becomes 23h00.5

Insomnia in children and adolescents

Paediatric insomnia is a widespread problem, ranging from 1%
to 6% in the general population and from 50% to 75% in children with
neurodevelopmental or psychiatric co-morbidities.6
The negative consequences of sleeplessness include hyperactivity,
irritability, restlessness, poor concentration, impulsiveness, suicide
risk and poor memory. Families of children with sleep disturbances also
suffer, exhibiting negative effects on daytime function and well-being,
as well as elevated levels of family stress.6
A useful definition is repeated difficulty with sleep initiation,
duration, consolidation, or quality that occurs despite age-appropriate
time and opportunity for sleep and results in daytime functional
impairment for the child and/or family. This includes children with
behavioural insomnia and those with insomnia that persists despite
proper sleep hygiene. Good sleep practices (avoiding caffeinated
beverages, age-appropriate sleep/wake schedules, and limit setting
regarding practices such as late night television viewing) and
behavioural strategies should be the first line of treatment.6

The three most important principles for treating bedtime resistance
in young children are: creating an emotional state of calmness and
safety, consistent limit setting and establishing good habits.5
Bedtime habits include a wind-down period and a sequence of activities
that begins 30 - 60 minutes before bedtime. If a child continues to
test limits and does not respond to strategies to reward desirable
behaviours, it may become necessary to set consequences for the
undesirable behaviours, e.g. the removal of privileges. However, this
can still be done within a positive framework to avoid the escalating
emotional arousals of screaming and flaring tempers.5
Pre-sleep onset worries and ruminative thinking at bedtime are a major
source of difficulty. The treatment principles include: helping the
child to feel emotionally and physically safe, addressing the worries
and establishing a regular bedtime routine. For adolescents, multiple
sleep-interfering factors (e.g. cell phones and the internet) may need
to be addressed. The adolescent with difficulty waking up for school
may be symptomatic of biological changes in the circadian system at
puberty which shift sleep-timing preferences in the direction of the
delayed sleep phase. Treatment requires gradual (15 min/day) alignment
of the sleep system to the desired schedule and then to maintain that
alignment. Avoid any daytime naps and be consistent during weekends and
holidays.5

One of the most contentious issues in the domain of treating
sleep problems in children and adolescents is the use of medication to
promote sleep onset.7
There are large numbers of medications prescribed by clinicians
including alpha agonists, antidepressants, atypical antipsychotics and
antihistamines. There is an absence of any empirical data on risks or
benefits for most of these medications. Weiss et al.
recommend combined sleep hygiene and melatonin as a safe and effective
treatment for initial insomnia in children with ADHD taking stimulant
medication.8
Short-term side-effects of melatonin in children are minimal but little
is known of the potential long-term effects, particularly on the
endocrine system. It should therefore be used cautiously in this age
group.

Conclusion

In adults, for the short-term treatment of insomnia where
there is a precipitant stressor, use a short course of hypnotics such
as zolpidem or zopiclone or a benzodiazepine. If the insomnia persists,
consider melatonin in those over age 55 years, non-nightly dosing of
the BZRAs and/or CBT. Further treatment may include the use of an
antidepressant. Continued failure of treatment suggests that referral
to a specialist may be appropriate. For children and adolescents,
behavioural intervention is the treatment of choice.